مقایسه تیپ شخصیتی D و سن بالاتر به عنوان همبستگی فاکتور اختلال نکروز توموری-α در نارسایی قلبی مزمن

Tumor necrosis factor-α (TNF-α) and its soluble receptors 1 (sTNFR1) and 2 (sTNFR2) have been shown to be implicated in the pathogenesis of chronic heart failure (CHF). Ageing is accompanied by increased plasma levels of pro-inflammatory cytokines. We hypothesized that Type D personality (joint tendency to experience negative emotions and to inhibit self-expression) and age may have similar pro-inflammatory effects in the context of CHF. Participants in this study were 130 consecutive outpatients with CHF (76% men); there were 70 relatively younger (⩽59 years) and 60 relatively older (⩾60 years) patients. They all completed the 14-item Type D Scale (DS14); 43 patients (33%) had a Type D personality. A multivariate model of cytokine levels indicated an independent overall effect of both older age [F(1, 128) = 9.11, p = .003] and Type D personality [F(1, 128) = 8.28, p = .005]. Stratifying patients in age/personality subgroups showed that younger non-Type D patients had the lowest and older Type D patients the highest sTNFR1 and sTNFR2 levels (986 ± 318 vs 1661 ± 1128 pg/ml and 1838 ± 777 vs 2823 ± 1439 pg/ml, p < .0001). Importantly, the mean sTNFR1 level in younger Type D patients (1359 ± 660 pg/ml) was equivalent to that in older non-Type D patients (1360 ± 440 pg/ml, p = .99) who were on average 18 years older. Younger Type D and older non-Type D patients also had similar sTNFR2 levels (2406 ± 1329 vs 2448 ± 812 pg/ml, p = .88). Only older Type D patients had a higher mean TNF-α level as compared to patients who were younger or who were not Type D (5.4 ± 2.9 vs 3.9 ± 2.4 pg/ml, p = .008). A logistic regression model including sex, severity of CHF, systolic heart failure and ischemic etiology indicated that the combined risk category of older age or Type D was independently associated with substantially increased sTNFR1 and sTNFR2 levels. Hence, Type D personality was associated with increased TNF-α activity. This disease-promoting effect of Type D matched the pro-inflammatory effect of ageing.

Chronic heart failure (CHF) is a rapidly growing medical and communal burden and its incidence rises sharply with increasing age (Mosterd and Hoes, 2007). This common cardiac condition carries a grim prognosis and severely impacts quality of life (Schiffer et al., 2005). The pathophysiological determinants of CHF are numerous and involve the activation of several neurohormonal pathways (von Haehling et al., 2004). The concept of CHF as a mere cardiologic entity has been modified, and it is now considered to be a multi-facetted systemic disease. It also entails several peripheral maladaptive processes, including skeletal muscle abnormalities and peripheral endothelial dysfunction (Conraads et al., 2002).